Neurologist Dr R. sits with Mr J., a 48-year-old photographer who’d recently suffered a stroke, in his office. Dr R. asks Mr J. to demonstrate a waving motion as if he were saying hello, to which he attempts with some difficulty. When asked to point towards the ceiling, Mr J. again encounters difficulties as he finds himself clenching and unclenching his fist. Dr R. proceeds to hold his hand out in front of him with his palm facing the floor. “Try to imitate the movement,” he asks. With deliberate effort, Mr J. eventually manages. “That’s good!” praises Dr R, “Now turn your hand over.” Mr J., with increased frustration, gives this a try – only to begin repeatedly slapping his hand against his thigh instead.
Mr J. is clearly trying to reproduce the movements that are asked of him, so what’s stopping him? Is it a generalised motor problem? This does not appear to be the case; as he’s asked to remove his glasses, Mr J. smoothly proceeds, and when asked to hammer a nail into a block of wood, Mr J. ably fulfills the request.
What Mr J. appears to suffer from is apraxia, “the difficulty in carrying out purposeful movements, in the absence of paralysis or muscular weakness” (Carlson, 2010). However, Mr J’s condition is a specific form of apraxia: ideomotor apraxia, whereby goal-directed movement is impaired – patients understand how to perform movements, but cannot carry them out. In this capacity, timing, sequencing, and spatial organisation of gestures are interrupted (Rothi & Ochipa, 1991). An example of a spatial error would be where, if the patient were asked to imitate brushing their teeth, they would use their fingers to represent the toothbrush (body-part-as-object substitution), or close their fist so tightly that there is no space for the imaginary toothbrush (orientation error). Interestingly, patients are still able to perform automatic actions when cued – this is known as the automatic-voluntary dissociation. Patients can use a telephone if they hear the phone ring, for example. This deficit, therefore, is less obvious in everyday life compared to in a clinical setting.
Ideomotor apraxia typically arises due to damage in the left parietal association areas and white matter bundles from the frontal and parietal association areas (Zadikoff & Lang, 2005). More rarely, other areas may also be involved such as the premotor and supplementary motor cortex, basal ganglia, and thalamus. Indeed, Dr R. states in his report, “The left parietal lobe is involved in the control of movements – especially sequences of movements – that are not dictated by the context. Thus, he finds it almost impossible to follow verbal requests to make arbitrary movements”. More specifically, Rushworth et al. (1997) suggest that the impairment in movement sequencing may be a result of a difficulty in redirecting motor attention from movement to movement in the sequence.
Although Mr J.’s motor independence was not as proficient as before, his apraxia is unlikely to have impacted his daily activities because patients are still able to respond to automatic actions that are cued. Nonetheless, speech and physical therapies and biofeedback exist to help patients regain some control (Smania et al., 2006; McNeil et al., 1976; Wambaugh et al., 2006). More interestingly, there is evidence to suggest that right hemispheric structures in the brain could compensate for the damage in left hemispheric structures which have led to motor problems (see Wheaton & Hallett, 2007). For example, the plasticity of higher brain areas may allow for the reorganisation of left parietal and premotor cortices with experience, and the relearning of certain activities that were previously reliant on the damaged areas (Kim et al., 2004). However, the mechanisms underlying this are not fully understood and we cannot completely determine whether the brain could compensate for the functions lost in apraxia.
This article was written by Manying Lo and edited by Robert Vilkelis. Both of them are members of the Bugle team.
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